Although the present study did not focus on activation of proinflammatory mechanisms as a causal mechanism for the progression of calcific aortic valve disease, Aikawa et al demonstrated that proinflammatory cathepsin S, a highly potent elastase, contributes to arterial and valvular calcification in mice with atherosclerosis and CKD assessed by in vivo and ex vivo optical molecular imaging [27]. The gene discussed is CTSS; the disease is aortic valve calcification.